Aleglitazar - CAS 475479-34-6
Not Intended for Therapeutic Use. For research use only.
Product Name:
Catalog Number:
R1439; RO0728804
CAS Number:
Aleglitazar is a potent dual agonist of peroxisome proliferator-activated receptor (PPAR) α/γ.
Molecular Weight:
Molecular Formula:
Chemical Structure
CAS 475479-34-6 Aleglitazar

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Reference Reading

1.Efficacy, safety and tolerability of aleglitazar in patients with type 2 diabetes: pooled findings from three randomized phase III trials.
Henry RR1, Buse JB, Wu H, Durrwell L, Mingrino R, Jaekel K, El Azzouzi B, Andjelkovic M, Herz M. Diabetes Obes Metab. 2015 Jun;17(6):560-5. doi: 10.1111/dom.12455. Epub 2015 Apr 8.
AIMS: To evaluate the potential efficacy, safety and tolerability of aleglitazar as monotherapy or add-on therapy to metformin or to a sulphonylurea (either alone or in combination with metformin).
2.Discontinued in 2013: diabetic drugs.
Hedrington MS1, Davis SN. Expert Opin Investig Drugs. 2014 Dec;23(12):1703-11. doi: 10.1517/13543784.2014.964859. Epub 2014 Sep 24.
INTRODUCTION: The increasing prevalence of diabetes, with no cure on the horizon, continues to provide biopharmaceutical companies with an incentive to develop novel therapies and improve existing compounds.
3.Differential effects of peroxisome proliferator-activated receptor agonists on doxorubicin-resistant human myelogenous leukemia (K562/DOX) cells.
Yousefi B1, Samadi N2, Baradaran B1, Rameshknia V3, Shafiei-Irannejad V4, Majidinia M4, Targhaze N5, Zarghami N6. Cell Mol Biol (Noisy-le-grand). 2015 Dec 30;61(8):118-22.
P-glycoprotein (P-gp)-mediated multidrug resistance (MDR) in tumor cells is still a main obstacle for the chemotherapeutic treatment of cancers. Therefore, identification of safe and effective MDR reversing compounds with minimal adverse side effects is an important approach in the cancer treatment. Studies show that peroxisome proliferator-activated receptor (PPARs) ligands can inhibit cell growth in many cancers. Here, we investigated the effect of different PPAR agonists include fenofibrate, troglitazone and aleglitazar on doxorubicin-resistant human myelogenous leukemia (K562/DOX) cells. The effects of doxorubicin (DOX) following treatment with PPAR agonists on cell viability were evaluated using MTT assay and the reversal fold (RF) values. Rhodamine123 (Rh123) assays were used to determine P-gp functioning. P-gp mRNA/protein expression was measured by quantitative reverse transcription polymerase chain reaction (qRT-PCR) and western blot analysis after incubation with troglitazone and aleglitazar.
4.The dual peroxisome proliferator-activated receptor alpha/delta agonist GFT505 exerts anti-diabetic effects in db/db mice without peroxisome proliferator-activated receptor gamma-associated adverse cardiac effects.
Hanf R1, Millatt LJ1, Cariou B2, Noel B1, Rigou G1, Delataille P1, Daix V1, Hum DW1, Staels B3. Diab Vasc Dis Res. 2014 Nov;11(6):440-7. doi: 10.1177/1479164114548027. Epub 2014 Sep 11.
We report here the efficacy and safety of GFT505, a novel liver-targeted peroxisome proliferator-activated receptor alpha/delta (PPARα/δ) agonist, in the db/db mouse model of diabetes. Mice were treated with vehicle, GFT505, PPARγ agonist rosiglitazone or dual-PPARα/γ agonist aleglitazar for up to 8 weeks. All compounds comparably reduced fasting glycaemia and HbA1c and improved insulin sensitivity. The glucose-lowering effect of GFT505 was associated with decreased hepatic gluconeogenesis, correlating with reduced expression of gluconeogenic genes. In contrast with the PPARγ-activating drugs, treatment with GFT505 did not affect heart weight and did not increase plasma adiponectin concentrations. This absence of cardiac effects of GFT505 was confirmed after 12 months of administration in cynomolgus monkeys, by the absence of echocardiographic and histological findings. Moreover, long-term GFT505 administration to monkeys induced no change in haematological parameters or in bone marrow differential cell counts.